Are you Akash Patnaik?

Claim your profile

Publications (3)17.35 Total impact

  • Article: The APL paradigm and the "co-clinical trial" project.
    [show abstract] [hide abstract]
    ABSTRACT: Tremendous advances in technologies have allowed the attainment of powerful insights into the molecular and genetic determinants that drive human cancers. However, this acquired knowledge has been translated into effective therapeutics very slowly, in part due to difficulty in predicting which drug or drug combination is likely to be effective in the complex mutational background of human cancers. To address this difficulty we have proposed and initiated the "co-clinical trial" project, in which we exploit mouse models that faithfully replicate the variety of mutational events observed in human cancers, to conduct preclinical trials that parallel ongoing human phase I/II clinical trials. Here, we focus on concepts relevant to the application of this novel paradigm and the essential components required for its implementation to ultimately achieve the rational and rapid development of new therapeutic treatments.
    Cancer discovery. 01/2011; 1(2):108-16.
  • Article: PI3K enters beta-testing.
    [show abstract] [hide abstract]
    ABSTRACT: Phosphoinositide-3-OH kinases (PI3K) are critical regulators of cell metabolism, growth, and survival. In a recent publication in Nature, Jia et al. (2008) identify specific functions of the p110beta isoform of PI3K in glucose metabolism, cellular proliferation, and tumorigenesis.
    Cell metabolism 10/2008; 8(3):179-81. · 17.35 Impact Factor
  • Chapter: Cancer Cell Metabolism
    [show abstract] [hide abstract]
    ABSTRACT: Human cancers result from multiple molecular aberrations, which act in concert with both the tumor microenvironment and metabolic macroenvironment to produce the malignant phenotype. Cancer cells exhibit fundamental differences in both anabolic and catabolic metabolism relative to their normal counterparts. Understanding cancer, the metabolic rewiring of cells that drives transformation may provide novel, selective therapeutic opportunities. This altered metabolism of cancer cells appears to be multifaceted involving the energy sensing machinery, as well as fatty acid, amino acid, and glycolytic metabolism. In this chapter, we describe several important features of the differential metabolism in cancer cells that may contribute to the development of a selective growth, proliferation, and survival advantage. We conclude with a summary of pharmaceutical interventions already in clinical use or currently under investigation that target this altered metabolism in human cancers.
    01/1970: pages 245-261;